Allergic contact dermatitis to urushiol (the allergen in poison ivy) is a common problem for which avoidance is often not practical.
Allergic contact dermatitis to the 15 or 17 carbon alkyl-substituted catechol oils present in poison ivy/oak & sumac and other plants of the Family Anacardiaceae (including cashew nut shells and mango fruit and sap), is a common source of chronic and recurrent morbidity among persons in rural and suburban parts of the eastern and central U.S. Immunotherapy with purified urushiol in olive oil was studied by both the oral route and by intramuscular injection in the 1970's. (Epstein W L, Baer H, Dawson C R & Khurana R C: Poison Oak Hyposensitization, Evaluation of Purified Urushiol. Arch Dermatol 1974 March; 109(3):356-60). Intramuscular (IM) injections were reported not tolerated because of local itch and rash, though the dose causing the reactions was not stated. Oral immunotherapy at cumulative doses of 100-677 mg reduced quantitative patch test reactivity but did not eliminate it, with loss of effect in the absence of weekly maintenance therapy. There were no treatment-associated abnormalities in CBC, urinalysis or basic blood chemistry and adverse effects were limited to transient, mild poison ivy-like eruptions in various body locations. These were controlled by “dose adjustment.”
Hyposensitization but not total loss of reactivity, persisting for 3 months without continuing maintenance therapy, was observed in 15 of 21 human subjects receiving a cumulative oral dose of 300 mg of the same formulation in a follow-up study. (Epstein W L, Byers V S, Frankart W.: Induction of antigen specific hyposensitization to poison oak in sensitized adults. Arch Dermatol. 1982 September; 118(9):630-3.)
The Hartley guinea pig can be sensitized to poison ivy and has been used as an animal model for poison ivy immunotherapy. ElSohly et al studied the immunotherapeutic response to diacetate esters of first natural and then synthetic poison ivy and poison oak urushiols in the Hartley guinea pig, his rationale being that the diacetate esters are “less toxic” on administration (by which he appears to mean less likely to provoke acute allergic contact dermatitis). He proposed that the esters are hydrolyzed by cell membrane esterases to release free and biologically active urushiol at sites at which it will be immunotherapeutic, so that one can deliver effective treatment doses more rapidly and eliminate the gradual build-up needed for immunotherapy with unesterified urushiol. He documented the effectiveness of 100 mg/Kg doses of urushiol given IV to guinea pigs as the diacetate ester in Arlacel emulsion, (Watson E S, Murphy J C, Wirth P W, Waller C W, & Elsohly M A: Immunologic Studies of Poisonous Anacardiaceae: I. Production of Tolerance and Desensitization to Poison Ivy and Oak Urushiols Using Esterified Urushiol Derivatives in Guinea Pigs. J Invest Dermatol 1981 March; 76(3)C64-70). He reported efficacy of the same dose of urushiol diacetate dissolved in corn oil and given by mouth, (Watson E S, Murphy J C & Elsohly M A: Immunologic Studies of Poisonous Anacardiaceae: Oral Desensitization to Poison Ivy and Oak Urushiols in Guinea Pigs. J Invest Dermatol 1983 March; 80(3): 149-55) and of 20 mg urushiol diacetate given IM in corn oil given either as a single dose or divided into 3 doses. (Walker L A, Watson E S & Elsohly M A: Single Dose Parenteral Hyposensitization to Poison Ivy Urushiol in Guinea Pigs. Immunopharmacology and Immunotoxicology 1995; 17(3), 565-576.) A mix of diacetate esters of poison ivy and poison oak urushiols given by mouth did not reduce quantitative patch test sensitivity at cumulative doses of either 306 mg or 1266 mg in poison ivy or poison oak-allergic humans. (Marks J G Jr, Trautlein J J, Epstein W L, Laws D M, Sicard G R: Oral hyposensitization to poison ivy and poison oak. Arch Dermatol. 1987 April; 123(4):476-8).